ArticleClinical immunology (Orlando, Fla.)2019
Taming hemodialysis-induced inflammation: Are complement C3 inhibitors a viable option?
Article in Clinical immunology (Orlando, Fla.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Biocompatibility in hemodialysis: artificial membrane and human blood interactions.BMC nephrology · 2025Review
- Unleashing the power of complement activation: unraveling renal damage in human anti-glomerular basement membrane disease.Frontiers in immunology · 2023Review
- Current status of COVID-19 among hemodialysis patients in the East Azerbaijan Province of Iran.Hemodialysis international. International Symposium on Home Hemodialysis · 2021Article
- Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury.International journal of biological sciences · 2021Review
- The first case of COVID-19 treated with the complement C3 inhibitor AMY-101.Clinical immunology (Orlando, Fla.) · 2020Article
- Prolonged intraocular residence and retinal tissue distribution of a fourth-generation compstatin-based C3 inhibitor in non-human primates.Clinical immunology (Orlando, Fla.) · 2020Article
- Clinical promise of next-generation complement therapeutics.Nature reviews. Drug discovery · 2019Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Owing to an increasing shortage of donor organs, the majority of patients with end-stage kidney disease remains reliant on extracorporeal hemodialysis (HD) in order to counter the lifelong complications of a failing kidney. While HD remains a life-saving option for these patients, mounting evidence suggests that it also fuels a vicious cycle of thromboinflammation that can increase the risk of cardiovascular disease. During HD, blood-borne innate immune systems become inappropriately activated on the biomaterial surface, instigating proinflammatory reactions that can alter endothelial and vascular homeostasis. Complement activation, early during the HD process, has been shown to fuel a multitude of detrimental thromboinflammatory reactions that collectively contribute to patient morbidity. Here we discuss emerging aspects of complement's involvement in HD-induced inflammation and put forth the concept that targeted intervention at the level of C3 might constitute a promising therapeutic approach in HD patients.
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Registered trials
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